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3C week 2 - ophthalmology > medical retina (see DM) > Flashcards

medical retina (see DM) Flashcards

1
Q

5 findings on fundoscopy of non-proliferative retinopathy

A
  1. microaneurysms;
  2. exudate;
  3. dot haemorrhages;
  4. blot haemorrhages;
  5. cotton wool spots
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2
Q

how does exudate form (diabetic retinopathy)

A

internal-retinal lipid deposits due to plasma leakage/oedema from microaneurysms or capillaries

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3
Q

how do cotton wool spots form (retinopathy)

A

axoplasmic debris from nerve-fibre infarcts - i.e. debris from death of nerve fibres

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4
Q

what is branch retinal vein occlusion

A

occlusion of a branch of the retinal vein as it is crossed by a retinal arteriole

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5
Q

what is central retinal vein occlusion (CRVO)

A

occlusion of vein in optic nerve as it runs alongside the central retinal artery

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6
Q

severe/ischaemic CRVO presentation

A

acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/60-hand motions only at 1m

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7
Q

severe CRVO retinal signson fundoscopy (5)

A
  1. severe intraretinal haemorrhages;
  2. engorged retinal veins;
  3. disc swelling;
  4. macular oedema;
  5. cotton wool spots
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8
Q

what clinical test will be +ve in severe CRVO

A

RAPD -> indicates severe loss of afferent visual input

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9
Q

3 complications of CRVO

A

rubeotic glaucoma; macular oedema; retinal neovascularisation

all are treatable

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10
Q

5 risk factors for CRVO

A
  1. age;
  2. HTN;
  3. arteriosclerosis;
  4. hyperlipidaemia;
  5. pro-thrombotic conditions
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11
Q

is the other eye at risk in CRVO

A

yes - the fellow eye may develop a retinal vein occlusion in 10% of people within 2-4yrs -> prevention by treating risk factors

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12
Q

mild/non-ischaemic CRVO presentation

A

acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/12-6/36

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13
Q

will RAPD be +ve in mild CRVO

A

no -> maintained afferent visual input

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14
Q

what changes occur to capillaries in CRVO and what does it lead to

A

damage to retinal capillary walls -> VEGF released -> leakage of plasma into the retina (macular oedema)

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15
Q

macular oedema treatment

A

anti-VGEF intravitreal injection

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16
Q

what does peripheral retinal ischaemia lead to (VGEF)

A

production of VGEF ->diffuses though the eye and stimulates growth of new blood vessels (rubeosis) on the iris and in the drainage angle -> can lead to angle closure glaucoma

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17
Q

how can rubeosis be treated

A

panretinal photocoagulation (PRP) - destroys ischemic retina, minimizes the eye’s oxygen demand, and reduces the amount of VEGF being released

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18
Q

branch retinal vein occlusion (BRVO) presentation

A

acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/9-hand movementd at 1m

may be asymptomatic if fovea not affected

19
Q

BRVO retinal signs (4)

A
  1. intraretinal haemorrhages in area of affected vein branch only;
  2. engorged branch retinal vein;
  3. macular oedema;
  4. cotton wool spots
20
Q

is RAPD +ve in BRVO

A

no - smaller area of retina involved than CRVO

21
Q

BRVO complications (3)

A

macular oedema; retinal neovascularisation; vitreous haemorrhage

22
Q

what is hypertensive retinopathy

A

damage to the retina due to HTN

23
Q

what can lowgrade hypertensionlead to

A

accelerated ateriosclerosis

24
Q

retinal signs of hypertensive retinopathy (4)

A

thickened arteriole wall; “silver wiring” - increased central light reflex; narrowed/straightened arterioles; AV nipping - thickened arteriole constricts the venule

25
Q

what is geographical atrophy

A

chronic progressive degeneration of the macula - loss of patches of choroid/ retinal pigment epithelium/ retina in an irregular shape

26
Q

what is amaurosis fugax

A

“fleeting blindness” - transient and sudden monocular blindness (like a curtain coming down)

27
Q

what can cause amaurosis fugax (2)

A
  1. carotid atheroma leading to emboli (fibrin-platelet/cholesterol);
  2. cardiac valve emboli (calcific) - rarer
28
Q

what assessment must be done post amaurosis fugax

A

stroke risk assessment - TIA clinic for carotid scan, ECG, anti-platelet

29
Q

what is the life expectancy for pts w CRAO

A

5.5 years

30
Q

retinal presentation of CRAO (4)

A
  1. pale retina/whitening - due to infarcted swollen inner 2/3 retina supplied by the CRA;
  2. “cherry red spot” - fovea -> no inner retinal covering fovea centre and photorecptors supplied by choroidal circulation;
  3. retinal artery narrowing;
  4. emboli may be present;
  5. boxcarring (segmental blood flow)
31
Q

4 causes of CRAO

A
  1. carotic atheroma - 90% of CRAOs are embolic in nature;
  2. calcified aortic valve lesions (emboli - rare);
  3. GCA (must rule this out!);
  4. traumatic vessel wall damage
32
Q

how can an embolus in the CRA attempt to be disloged

A

by lowering IOP -> aids the perfusion pressure gradient (usually ineffective)

33
Q

GCA symptoms (8)

A
  1. headache;
  2. temporal/scalp tenderness;
  3. jaw claudication;
  4. systemic symptoms (fever, lethargy malaise);
  5. transient vision loss;
  6. permanent ischaemic optic neuropathy;
  7. retinal artery occlusion;
  8. temproal artery thickening/tender/pulseless
34
Q

3 tests for GCA

A
  1. BLOODS (raised ESR, CRP, platelets);
  2. carotid ultrasound;
  3. temporal atery biopsy
35
Q

is retinal artery occlusion an emergency?

A

yes - immediated systemic evaluation and referral to TIA service required

36
Q

what may patients who have CRAO concurrently present with

A

silent ischaemic stroke

37
Q

5 risk factors for retinal artery occlusive disease

A
  1. older age (>70%);
  2. diabetes mellitus;
  3. arterial hypertension;
  4. ischaemic heart disease;
  5. smoking
38
Q

CRAO vs BRAO presentation

A

CRAO - Loss of vision over entire field;
BRAO - hemi field defect (or may even have 6/6 vision if cilioretinal artery sparing)

39
Q

what vessels are usually involvedin BRAO

A

temporal retinal vessels

40
Q

BRAO treatment

A

does not usually require treatment unless perifoveolar vessels are threatened

41
Q

CRAO/BRAO investigations

A
  1. FBC for anaemia, polycythemia, platelet disorders etc. ;
  2. ESR/CRP for inflammatory ateritis;
  3. fribrinogen levels, anti-APPL, aPTT, serum protein coagulopathies;
  4. cholesterol, triglycerides, lipids for atherosclerotic disease;
  5. echo/ECG for valve disease or AF;
  6. blood cultures - bacterial endo/septic emboli
42
Q

2 managements fro RAO in emergency care

A
  1. ocular massage - disloges the embolus to a point further down the arterial circulation and improves retinal perfusion;
  2. anterior chamber paracentesis - if visual loss has been present <24hrs, slit-lamp removal of 0.1-0.4mL of aqueous humour to decrease IOP -> allows greater perfusion and embolus to be pushed further down the vascular tree
43
Q

medical therapy for CRAO

A

treatment is directed towards lowering IOP, increasinf retinal perfusion and increasing oxygen delivery to hypoxic tissues

  1. timolol (start early);
  2. acetazolamide + mannitol;
  3. carbogen therapy (5%CO2, 95% O2) -> CO2 dilated retinal arterioles and O2 increases oxygen deliveryto ischaemic tissues;
  4. hyperbaric oxygen therapy (if initiated within 2-12hrs)

3C week 2 - ophthalmology (6 decks)

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